Inflammatory Arthritis - RA

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RA Facts

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Arthritis means inflammation in the joint. Inflammation is painful and is a very common medical problem. Arthritis is not the same as arthralgia,aches and pains many people have upon awakening or after exercising. If aches and pains are like a light summer breeze,arthritis is like a storm,and rheumatoid arthritis is like a hurricane.

Arthritis can be classified as either inflammatory or non-inflammatory. Inflammatory arthritis features inflammatory white blood cells in the joint fluid Forms of inflammatory arthritis includes RA,lupus arthritis,gout and many others. Forms of non-inflammatory arthritis include osteoarthritis,arthritis of thyroid disease, arthritis after injury,and many others.

Symptoms of RA differ considerably from those of other types of arthritis,such as gout and OA. e.g.,gout tends to cause intermittent joint inflammation with a sudden onset,and episodes last only a few days. OA,on the other hand,tends to cause chronic use-related pain. In addition OA is associated with minimal or no inflammation and involves fewer joints than does RA. Morning stiffness,a typical feature of RA,is uncommon in OA.

Sixty-five percent of the senior population have the degenerative or "wear-and-tear" type of arthritis. OA can also result because of injury or trauma to a joint. Some patients will not require medication,and others may even be unaware of the condition except when radiographic pictures are taken. While other patients may require surgical procedures to be performed. Severity will depend on individual case and type. Osteoarthritis is usually a localized condition, resulting in damage to cartilage. It is thought that if one lives long enough 90% will have some form of osteoarthritis.

There are more than 100 known types of arthritis. RA is the most disabling form of arthritis, osteoarthritis,some think is the only type of arthritis around, gout is usually not associated with arthritis by many people,lupus can be mild, and quickly go into remission or be serious and life-threatening depending on case and type,and there are pain sydromes like fibromyalgia which are common,while others are rare.

One important way to distinguish RA from other forms of arthritis is by the pattern of joint involvement. e.g.,RA usually affects the wrist and many of the hand joints,but often not the joints that are closest to the fingernails. Osteoarthritis,in contrast,affects those joints closest to the fingernails more often than other areas of the hand. In RA,the joints tend to be involved in a symmetrical pattern. i.e.,if the knucles on the right hand are inflamed,the knucles on the left hand are more likely to be inflamed as well.

Rheumatoid arthritis is an autoimmune disorder of unknown cause characterized by symmetric,erosive synovitis,and often mutisystem involvement. Most patients exibit a chronic changinging course of disease that if left untreated may result in progressive joint destruction, deformity, disability,and possible premature death. RA is one of the most common and serious type of arthritis. It affects all ages and races. RA affects approximetly 1% of the population and this low prevelance may mean that many health care professionals may have little experience in treating the disease successfully.

The inflammation associated with RA also may occur outside the joints. These inflammatory changes are called extra-articular features (EAFs). Extra-articular feaatures are found more common in patients with moderate-severe types of RA,but they can occur in all types. Since RA can cause EAFs,it can be viewed as a disease that affects the whole body,not just joints. The eyes, heart,lungs,blood-vessels,nerves etc.,can be involved.

Although we do not know the cause of rheumatoid arthritis,joint damage is caused by inflammation in the synovial membrane. This normally thin memberane becomes inflamed and thick,filled with cells called fibroblasts,lymphocytes,polymorphs, and macrophages. This thick,inflamed synovial membrane is called the pannus. The cells within the pannus becomes activated,and releases enzymes,and chemicals that both permanetly damage the cartilage and the bone,and also attract more cells into the inflamed tissue. In RA,this inflammatory process is like a one-way highway, the inflammation continue indefinitely causing more and more damage,possibly leading to joint destruction,and deformity if not controlled.

This inflammatory process is part of the body's immune system. The immune system is a natural defense against invaders such as bacteria, viruses,and even cancer. The cells of the immune system recognize,and respond to invaders either by making antibodies to combat invaders or by attacking invaders directly.

Although the immune system is normally activated by a foreign agent,it can be activated to attack normal cells. In RA,for unknown reasons,the immune system becomes over-activated and causes marked inflammation in the synovial membrane. Many of the drugs used to fight RA have antibacterial and/or anti-immune system activity.

The damage to the joints caused by RA is thought to be caused by the interaction of many inflammatory cells and chemicals. Cytokines,like tumour necrosis factor,IL-ra alpha etc., are secreated by synovial fibroblasts and other cells resulting in pain,and inflammation TNF may also be responsible for influencing other inflammatory compounds including interleukins (IL-1), collagenase,and prostaglandins

Complete remission is defined as the absence of
 
1) symptoms of active inflammatory joint pain (in contrast to mechanical joint pain).
 
2) morning stiffness.
 
3) fatigue.
 
4) synovitis on joint examination.
 
5) progression of radiographic damage on sequential radiographs. 6) elevated erthrocyte sedimintation rate or (ESR),or C-reactive protein (CRP) level. If complete remission is not achieved,the management goals are to control disease activity,alleviate pain,maintain function for essential activities of daily living,and work,maximize quality of life,and slow the rate of joint damage.

Typical symptoms:
 
*Pain,swelling,limited motion,warmth,and tightness around involved joints,most commonly,including the hands,and wrists,feet and ankles, elbows,shoulders, neck, knees,and hips,usually in a symmetric pattern, over time,joints may form deformities.
 
 *Generalized fatigue,soreness,stiffness,and aching,particularily in the early morning,and afternoon (described as morning stiffness,and afternoon fatigue).
 
*Lumps or rheumatoid nodules below the skin (moderate-severe RA)
 
 *Weight loss.
 
*Low grade fever,and sweats.
 
*Sleep difficulties.
 
*Weakness,and loss of mobility.
 
 *Depression (may worsen existing disease or provoke it as a new problem).

There are three basic classes or types of RA mild,moderate and severe. Ten percent of RA patients have a form of arthritis characterized by stiffness rather then swelling. These patients may have no deformity but their day-to-day function will be profoundly affected.The effects, medication,treatment and future course is different in each individual case.Presently there is no cure for RA but there has been many recent advances in F.D.A. approved medications that was not available in the past.

With the help of a rheumatoligist,and by doing one's personal,selected research,most patients will lead a normal, active, controlled,self- manageable,life according to his or her personal capabilities and limitations.The prognosis is mainly up to the patient.

The major underlying feature of RA is inflammation. By controlling inflammation,not only can the symptoms of RA be alleviated,but permanent disability can be prevented or minimized.

Three different types of drugs help combat inflammation. NSAIDs (non-steroidal anti-inflammatory drugs)help in controlling the symptoms of RA but do not stop the on-going progressive destruction that continues in rheumatoid arthritis. DMARDs (disease modifying drugs) are designed to help stop progression of the x-ray damages that occurs to ligaments,bone etc. Steroidal drugs such as predisone are used since some DMARDs may take up to six months to show its effects. Long term steroidal medication is not recommended because it has serious side effects such as osteoporosis (thins the bone). It serves as a effective "bridge" before the effects of the DMARDs come into play. Steroid drugs such as predisone are "fast-acting".

NSAIDs alone may be prescribed in the mild cases but DMARDs and NSAIDs are required in the moderate and severe cases. Biologic drugs have been developed to combat T.N.F. (tumour necrosis factor) a prime mediator of inflammation but the cost factor is the main draw-back currently.

Recently another drug was approved by the (F.D.A.)Federal Drug Administration to combat another cytokine IL-1 also involved in the inflammatory process. There are currently many research projects going on to combat rheumatoid arthritis.

The help of specifically trained health care workers in rheumatic diseases will help in the management and treatment of RA. The major aim of treating RA is to control the inflammation before erosive and destructive forcess come to play in the disease process.

If the ("fire") inflammation of RA is controlled,pain,and swelling will diminish,and damage and possible deformity will be limited. Limited from inflammation,the patient will be able to resume a more satisfying,and productive life-style.

The patient will have the greatest interest in getting the most effective treatment for RA disease control. To accomplish this goal,the arthritis must be diagnosed promptly,and its type determined. A knowledgeable,and compassionate physician who is able to select,and recommend the most appropiate treatment is a essential component of the whole disease control process.

Patients must take resposibility for their own disease,and navigate through the health care system to ensure the disease gets the treatment it needs. The "window of opportunity" to control the disease,when the disease is more manageable (2 years-onset of disease)exists,but it is never to late,to initiate DMARD therapy.

The American College of Rheumatology has set up guidelines in the diagnosis of RA,and that patients meet 4 of the 7 criterias.
 
1)Morning stiffness lasting one hour. In fact,even stiffness lasting more than 30 minutes suggests inflammatory disease presence, continued activity will aggravate the problem,and exacerbate the pain.
 
2) Swelling in 3 or more joints simultaneously.
 
3) Swelling in the hand joints (PIP,MCP,or wrist).
 
4) Symmetric arthritis initially,joints on one side of the body may be involved,but the arthritis tends to spread to the other side of the body.
 
5) Erosions or decalcifications on x-ray of the hand.
 
 6) Subcutaneous rheumatoid nodules.
 
7) A positive serum rheumatoid factor assay. These are guidelines set up under laboratory conditions and some RA patients may not meet the suggested criteria (mild RA patients). Other patients will have a negative RF,and rheumatoid nodules will not appear on all RA patients.

The current American College of Rheumatology (ACR) guidelines for the treatment of RA begin with establishment of diagnosis, determination of disease activity, and development of a prognosis. Therapy is initiated with patient education and physical therapy, disease-modifying antirheumatic drug(s) (DMARD), and perhaps corticosteroids and/or a nonsteroidal anti-inflammatory drug (NSAID).
 
If the response to treatment is not adequate after 3 months, therapy should be altered by changing or adding DMARDs, either as monotherapy or in combination. Biologic DMARDs should also be considered either alone or as add-on therapy.
 
Patients who still do not respond adequately despite being on several DMARD regimens are considered multiple DMARD failures. These patients will continue to have signs and symptoms and progression of structural joint damage.
 
The relationship between the development of radiographic joint destruction in RA and its long-term consequences for the patient is not well understood, but one view of the disease process is that inflammatory joint symptoms are the main determinant of disability early in the disease, while joint destruction dominates in late disease.
 
Presentations and discussions at OMERACT IV (the 4th International Consensus Conference on Outcome Measures in Rheumatoid Arthritis Clinical Trials) are consistent with this view, suggesting a high correlation between inflammation and disability in early RA, but that the strength of this relationship declines over time. Discussions at OMERACT IV also indicated that fluctuations in disability will become less pronounced in later-stage RA and become more closely correlated with radiographic evidence of joint damage.
 
Progressive joint damage occurs in unchecked RA. In the early stages of the disease, cartilage destruction begins, and neutrophils, T cells, and B cells are recruited into the synovial cavity. The synovial membrane exhibits hyperplasia, and hypertrophic synoviocytes and capillaries are starting to form. In a joint with established RA,the greatly thickened, inflamed synovium (pannus) invades and erodes adjacent bone and cartilage. Activated macrophages, lymphocytes, and fibroblasts and their products stimulate extensive angiogenesis, a central feature in synovial inflammation and pannus formation. Synovial villi become evident.
 
TNF-alpha is one of the most potent osteoclastogenic cytokines produced in inflammation, and it is pivotal in the pathogenesis of RA. Production of TNF-alpha and other proinflammatory cytokines in RA is largely T-cell dependent. Activated synovial T cells express both membrane-bound and soluble forms of RANKL. In the RA synovium, fibroblasts also provide an abundant source of RANKL and macrophage colony-stimulating factor (M-CSF).
 
TNF-a and IL-1 target stromal-osteoblastic cells to increase expression of RANKL. In the presence of permissive levels of RANKL, TNF-alpha acts directly to stimulate osteoclast differentiation of macrophages and myeloid progenitor cells.  In addition, TNF-alpha induces IL-1 release by synovial fibroblasts and macrophages, and IL-1, together with RANKL, is a major survival and activation signal for nascent osteoclasts. Thus, TNF-alpha and IL-1, acting in concert with RANKL, can powerfully promote osteoclast recruitment, activation, and osteolysis in RA.
 
Cytokines exert their damaging effects by binding to specific receptors, and there are several potential approaches that can be employed to block these effects. Cytokines can be neutralized through the use of antibodies or soluble receptors. With this approach, the cytokine never reaches the receptor on the cell of interest. This avenue for the treatment of RA has been taken with soluble TNF-alpha receptor fusion proteins, soluble IL receptors, monoclonal antibodies against TNF-alpha, and monoclonal antibodies against IL-6.
 
Receptor antagonists or antibodies can bind to cytokine receptors on cells and prevent cytokines from binding. This blocks their actions on the cell in question. This approach to the treatment of RA has been taken with recombinant IL-1Ra and an antibody against the IL-6 receptor. Administration of anti-inflammatory cytokines can inhibit expression of inflammatory cytokines. This approach has been taken with IL-4 and IL-10.
 
Cytokines have a very wide range of functions relevant to the pathophysiology of RA. Functions relevant to RA; Regulation of the inflammatory respomse; a)Proimflammatory: TNF-alpha,IL-1,IL-6.IL-7,chemokines (Il-8,MIP1 alpha/beta,Rantes) b) Anti-inflammatory: IL-10,TGF-beta,IL-4,IL-1Ra,sTNFR I/II,IL-1R II
 
Modulation of the immune response; I) Modify Th1/Th2 bias ;a) Th1:IL-12,IL-18,IFN-y ;b) Th2:IL-4,Il-13,IL-10,chemokines  II) Mediate activation/apoptosis: IL-2,IL-15,IFN-y,IL-3,IL-5,IL-7,
 
Remodel tissue; I) Bone and cartilage destruction: IL-1,TNF-alpha,OPG/RANKL (TRANCE) ;II) Angiogenesis/growth factors: TNF-alpha,TGF-beta,VEGF
 
These molecules are key regulators of inflammatory responses, having actions that are either proinflammatory (TNF-alpha, IL -1, IL-6, IL-7, chemokines, IL-8, MIP-1alpha/beta, and regulated upon activation, normal T cell expressed and secreted [RANTES]) or anti-inflammatory (IL-10, transforming growth factor [TGF]-beta, IL-4; IL-1 receptor antagonist [Ra], soluble TNF receptor [sTNFR] type I/II, and type II IL-1 receptor [IL-1R II]).
 
Cytokines can also modulate immune responses. IL-12, IL-18, and interferon (IFN)-y promote a Th1 bias and IL-4, IL-13, IL-10, and chemokines promote a Th2 bias. Activation and/or apoptosis are mediated by IL-2, IL-15, IFN-y, IL-3, IL-5, and IL-7. Cytokines are also involved in regulation of tissue remodeling. IL-1, TNF-alpha, and OPG (osteoprotegerin) /RANKL (receptor activator of nuclear factor-kappa b ligand) (TRANCE, TNF-related activator-induced cytokine) have been implicated in bone and cartilage destruction, and TNF-alpha, TNF-beta, and vascular endothelial growth factor (VEGF) have been shown to have trophic/angiogenic effects.
 
CD4+ T cells might initiate the disease process in RA. Activated by antigens, these cells stimulate monocytes, synovial fibroblasts, and macrophages to produce the key proinflammatory cytokines TNF-alpha, IL-1, and IL-6 as well as to release MMPs, enzymes that degrade connective tissue matrix.1 TNF-alpha and IL-1 also inhibit synovial fibroblasts from producing tissue inhibitors of MMPs. These two actions by TNF-alpha and IL-1, among others, are believed to result in the joint damage that occurs in RA. Activated CD4+ T cells also contribute to joint damage by stimulating the development of osteoclasts by expressing osteoprotegrin ligands (OPGLs) and by stimulating B cells to produce immunoglobulins such as rheumatoid factor.
 
Activated macrophages, lymphocytes, and fibroblasts and their products can stimulate angiogenesis, a fact that may account for the increased vascularity of the synovium in rheumatoid joints. Other cytokines involved in the complex cellular interactions that occur as part of the inflammatory process include IL-4, IL-10, IL-12, and IFN-g. In addition, CD11 and CD69 cells are involved in the cell-surface signaling that leads to the production of cytokines.
 
Research investigators analyzed the direct medical care costs for RA over 1- and 11-year periods, and assessed the impact of poor function and functional decline on these expenses. Their analysis used data from the University of California, San Francisco, RA Panel Study in which 1,156 patients were followed for up to 15 years.
 
Medical care costs for RA for 1995 to 1996 averaged $5,919 per patient. Hospital admissions contributed 51.7% of this total and drugs contributed 26.1%. The respective contributions for physician visits, allied health professional visits, testing, and other expenses were 8.6%, 1.4%, 4.7%, and 7.5%.

In an era of increased scrutiny of both costs and quality, health outcomes research has become a focus of attention in many areas of medicine. In an effort to improve healthcare outcomes, it is first necessary to define and measure "quality." Although both the definition and measurement of quality remain a source of continued debate, the Institute of Medicine defines quality as the "degree to which health services for individuals and populations increase the likelihood of desired health outcomes and are consistent with current professional knowledge." Lack of quality can be due to overuse, underuse, or misuse of resources. Although this definition is a useful starting point for discussion, it does not incorporate the additional important dimension of patient values or preferences.
 
In 1966, Donabedian first proposed a conceptual framework that has remained useful in evaluating the quality of healthcare. Using this theoretical construct, factors that contribute to quality are separated into 3 groups: those affecting structure, process, or outcome. Structural measures pertain to the capacities, technologies, and infrastructures that make up the organization of a healthcare system. Process is defined as what is done for or to the patient and may be administrative, clinical, or financial (eg, periodic laboratory monitoring for patients receiving disease-modifying antirheumatic drug [DMARD] therapy). Optimal process measures can often be associated with positive outcomes by examining results from clinical trials.
 
Patient outcomes are the end point of greatest interest and include mortality, morbidity, and functional status. Outcomes may be relatively easy to measure in carefully controlled clinical trials focused on "efficacy." However, it is much more difficult to measure outcomes in real-world "effectiveness" studies involving populations or health systems or within a physician's office.
 
Moreover, due to varying demographics and burdens of disease among patient populations, directly measuring outcomes may be costly, time-consuming, and not sensitive enough in detecting differences in the quality of healthcare provided.
 
In contrast to outcomes, process of care is more easily evaluated, requires shorter end points, offers higher sensitivity in detecting differences among treatments provided, and usually requires no risk adjustment.
 
Implicit in the evaluation of the structure of healthcare is that patients must have good access to care. Lacaille and colleagues studied 29,297 individuals with rheumatoid arthritis (RA) in British Columbia, Canada, from 1996 to 2000. RA was defined by at least 2 physician visits at least 2 months apart and no other connective tissue disease diagnosis. These investigators found that only 32% of patients had seen a rheumatologist in this 5-year period (range, 9% to 38%, depending on province), whereas the majority (53%) were followed up only by a general practitioner. Of those seen by a rheumatologist, 80% had received DMARDs compared with only 14% of patients seen by a family physician.
 
Presenting the results of a recent North American RA study, Sokka and Pincus reported on a cohort of 296 RA patients, pointing out that most of them (> 60%) had not been seen by a rheumatologist until at least 4 months after the onset of their symptoms. Those with longer disease duration before evaluation and treatment were more likely to be seropositive for rheumatoid factor and to have erosive disease as well as worse pain and health status.
 
In a third investigation, Kwoh and colleagues studied 944 RA or inflammatory polyarthritis patients in 2001 and found that only half of them had ever seen a rheumatologist, and, consistent with the British Columbia study, DMARD use varied greatly between those having seen a rheumatologist (64%) and those not having seen a rheumatologist (27%). Patients treated by rheumatologists were 50% more likely to be prescribed selective cyclooxygenase 2 inhibitors (coxibs), and 25% were less likely to be treated with narcotics.
 
In addition to barriers to seeing arthritis specialists in a timely fashion, barriers to receiving newer, more effective, or safer drugs may adversely affect health outcomes. One of the most exciting developments in rheumatology is the addition of biologic agents, including tumor necrosis factor (TNF) inhibitors, to the armamentarium of agents used to treat active inflammatory disease.
 
Another newer class of drugs, coxibs, has made nonsteroidal anti-inflammatory drug (NSAID) therapy safer and, thus, more rational for high-risk patients by reducing gastrointestinal morbidity. However, the expense of drugs in both these classes is much greater than their older counterparts, and administrative barriers to receiving these agents imposed by health plans may negate their expected health benefit in high-risk patients.
 
Yelin analyzed data obtained from 493 patients and found that patients in health maintenance organizations (HMOs) were only half as likely to receive TNF-blocking agents and 40% less likely to receive coxibs compared with those in fee-for-service plans. Since prior work has shown a negligible difference between healthcare utilization rates of other resources (eg, outpatient visits) among different types of health plans, it appears that controlling costs by restricting access to newer medications is a cost-saving strategy that may be used by some HMOs.
 
Briesacher and colleagues studied 38,072 RA and osteoarthritis patients in 2000 and found that coxib use declined dramatically as copayments increased. Of patients in a 1-tier plan (average copayment, $8), 63% received coxibs compared with only 9% of patients in 3-tier plans (average copayment, $72).
 
Another important health service research question is whether the use of both traditional and biologic DMARDs is improving long-term health outcomes. Large, population-based studies and registries provide important effectiveness data to help answer this question.
 
Bombardier and colleagues reported on the Study of New Onset Rheumatoid Arthritis (SONORA) cohort of 1000 North American and Canadian patients with early RA and found that 79% of RA patients enrolled > 3 months after diagnosis had received DMARDs. Those patients who had not received DMARD therapy (35% in the overall cohort) had more active disease (as measured by the Health Assessment Questionnaire, global pain, and physician- and patient-determined disease assessments) and higher tender and swollen joint counts. These findings are timely given the emerging evidence that early evaluation by a rheumatologist and institution of early and aggressive DMARD therapy, more commonly implemented by rheumatologists than generalists, may retard radiographic disease progression and delay adverse outcomes in some patients.
 
Despite the increasing clinical trial evidence about the efficacy of TNF-blocking agents, long-term health outcome effectiveness data have been lacking. Kvien and colleagues studied almost 1000 RA patients in Oslo, Norway, served by 1 hospital and 1 outpatient facility from 1994-2001. The use and type of resources provided to this population did not significantly differ in any way over time except for increased access to new medications, including coxibs and TNF-blocking agents. Physical health status, pain, and global scores were improved from 1996-2001 and were attributed to the access to these new agents. Incorporating data on the incremental costs associated with use of these drugs during this period, these investigators found that cost per quality-adjusted life-year gained was US $29,000, a value comparable to that of other commonly advocated medical therapies.
 
Although identifying and ultimately ameliorating disparities in access to specialist care and to new therapies is a continuing and important issue in outcomes research, another area addresses inefficiencies owed to individual physicians. Given the national shortage of rheumatologists, methods to minimize waiting periods for patient access to arthritis specialists are particularly warranted.
 
Newman and colleagues reported on their efforts to "do today's work today" and convert a typical office-based rheumatologist practice with excessive waiting times for a new consultation to an "open access model," where between 6 and 8 hours of unscheduled clinic visits were available each day for either same-day new patient or follow-up visits. New patients were able to see a rheumatologist within days of referral. Follow-up patients were given a return appointment date only if they needed to be seen within 3 months, but if their expected follow-up was > 3 months, they were told which week to make their appointment; they would call the day or week of the desired appointment and would be seen in the next 72 hours. Internet-based algorithms were created and made accessible to referring primary care physicians for common problems  (eg, knee osteoarthritis) that enabled the primary care physicians to manage routine complaints more effectively and to guide the diagnostic studies obtained before the referral.
 
These algorithms included management strategies, Web-based links, and a series of predefined order sets that could be customized for an individual patient, allowing the physician to choose patient education resources, assisting devices, physical therapy, medications, and radiographs. Newman's group was able to reduce the third available appointment from 60 days to fewer than 2 days. Cancellations decreased from 40% to less than 15%, and both physician and patient satisfaction rose. Net revenues increased, and both total referrals and referrals of patients with active inflammatory disease (largely RA) increased by approximately 50% compared with a similar period historically.
 
The structure of healthcare provided and an adequate access to that structure are integral in achieving improved equity and efficiency. The above research provides valuable information at a population, health plan, and office level about overcoming the barriers to early evaluation and treatment of patients with active inflammatory disease. Other research data presented at ACR this year showed that in the real world aggressive arthritis treatment can lead to improved outcomes at a cost that is acceptable.
 
It is difficult to define treatment algorithms and clinical practice guidelines for disorders of unknown pathogenesis and, often, unclear diagnostic criteria. Nonetheless, different expert groups periodically assemble consensus panels to try and define appropriate care criteria. As an example, the ACR issued guidelines for RA in 2002.  These guidelines recommend initial therapy with a traditional DMARD for at least 3 months at maximal dosing (methotrexate, 25 mg/wk) before prescribing an anti-TNF agent.
 
In an effort to define appropriate and inappropriate use of anti-TNF therapy, Berger and colleagues reviewed the results obtained in 4124 RA patients receiving TNF-blocking therapy (infliximab or etanercept) covered by Caremark during a recent 1-year period to determine whether the patients had been given DMARD therapy in the period preceding administration of anti-TNF agents. They found that only 22% of patients had received a traditional DMARD before biologic therapy, and only 17% had been treated according to the ACR recommendations for the use of biologic agents, as outlined above.
 
 Although no set of recommendations can or should be interpreted as the standard of care for any individual patient, the use of biologics as first-line drugs in approximately 80% of patients may represent overzealous use, given available data and their expense.
 
For the first time, the ACR devoted an entire oral symposium to measuring the quality of care in rheumatic disease. A major theme of this session was the development of quality indicators (QIs). QIs are process-of-care measures that identify a discrete population and define a health service that should be performed for that population. They differ from practice guidelines in that they are very specific and usually constitute a minimal standard of care for all patients in a well-defined population.
 
In contrast, practice guidelines tend to be broader, often take the form of "should be considered," and are not necessarily applicable to an individual patient. Moreover, QIs can be developed for patients who might be traditionally prohibited from participation in clinical trials due to strict exclusion criteria, such as age or comorbidities, making QIs useful in a real-world practice.
 
Using a process outlined previously, Mikuls and colleagues defined minimal standards of care for gout management. These researchers developed QIs using a systemic literature review and refined them further by convening 2 sequential panels of content experts. Their ongoing work is characterizing factors associated with adherence to these QIs.
 
Pencharz and associates used previously defined osteoarthritis-specific QIs developed by the Assessing Care for Vulnerable Elders (ACOVE) project to study 323 patients with OA. Although pharmacologic process-of-care measures were higher than nonpharmacologic ones, quality scores (proportion of eligible patients receiving the process of care) were, overall, suboptimal. First-line osteoarthritis therapy was acetaminophen for 60.4% of patients, and 79.5% of acetaminophen-treated patients were taking the maximal dose before switching to NSAIDs. However, only about a quarter of new and established patients with osteoarthritis received patient education, and exercise therapy for new and established osteoarthritis was prescribed to only 29% and 40.1% of patients, respectively.
 
The development of QIs and assessment of adherence are necessary first steps in improving the care provided to patients. In an era where standardized performance measures, such as the Health Employer Data Set, are used to compare health plans and allow purchasers to make informed decisions about where to spend their healthcare dollars, it is likely that QIs of process of care will be increasingly used to assess both health plan and physician performance and to determine whether they are conforming to appropriate standards of care. Some health plans have already begun establishing incentive programs that could be linked to reimbursement for physicians who consistently demonstrate excellent quality of care.